J Formos Med Assoc
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Multicenter Study
Long-term usage of narcotic analgesics by chronic intractable noncancer pain patients in Taiwan from 2003 to 2012.
Chronic pain is a common and important medical problem worldwide. Patients with chronic intractable noncancer pain (CINCP) are treated primarily with narcotics. We analyzed the characteristics of patients with CINCP and the pain prescriptions of Taiwan's physicians. ⋯ To decrease malaise and addiction in patients with CINCP, Taiwan's physicians need more education on narcotic analgesics, and greater professional cooperation to develop therapeutic guidelines that will improve pain care for patients with CINCP.
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Mutations in the tet oncogene family member 2 gene (TET2) are frequently found in adult patients with acute myeloid leukemia (AML). Reports of TET2 mutations in children are limited. We assessed the prevalence of TET2 mutations in Taiwanese children with AML and analyzed their prognosis. ⋯ The prevalence of TET2 mutations in children with AML compared with adults with AML was lower and less complex. Patient prognosis associated with TET2 mutations in children requires further investigation.
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Parkinson's disease (PD) is the second most common neurodegenerative disorder worldwide. Although idiopathic PD accounts for most of the cases, several genetic mutations have been found to cause PD. Mutations in the eukaryotic translation initiation factor 4-γ, 1 (EIF4G1) gene have been identified since 2011, which were reported to be associated with PD among Caucasians in subsequent research. However, this observation was not consistent. The contribution to other ethnic groups remains limited, with < 1% of sporadic cases. We conducted a case-control study to analyze if EIF4G1 is a risk factor for PD patients in Taiwan. ⋯ This study indicates that the EIF4G1 mutation is rare in Taiwan, which is consistent with other reports from Asia. Ethnicity could have a great influence on EIF4G1 in PD. Further large scale studies are warranted to evaluate the association of PD and EIF4G1 gene.